Evidence map›Paper›PMID 16201018›Full record

ArticlePLoS pathogens2005

Natural variation in Vif: differential impact on APOBEC3G/3F and a potential role in HIV-1 diversification.

Viviana Simon, Veronique Zennou, Deya Murray, Yaoxing Huang, David D Ho, Paul D Bieniasz

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
173citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

173 citing papers in PubMed, 1 synthesis or guideline pooled it, 249 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Fitness Landscapes of APOBEC3G Antagonism by HIV-1 Vif proteins.bioRxiv : the preprint server for biology · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. HIV-1 Vif protein sequence variations in South African people living with HIV and their influence on Vif-APOBEC3G interaction.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2024
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Characterization of an A3G-VifMolecular & cellular proteomics : MCP · 2021
    Article
  17. Article
  18. Article
  19. Article
  20. Article

113 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Viviana SimonAaron Diamond AIDS Research Center, The Rockefeller University, New York, New York, United States of America. vsimon@adarc.org
Veronique Zennou
Deya Murray
Yaoxing Huang
David D Ho
Paul D Bieniasz
Aaron Diamond AIDS Research Center · USRockefeller University · US

Funding

RNA Protein interactions in HIV-1 replicationR01AI050111 · NIAID · ROCKEFELLER UNIVERSITY · PI BIENIASZ, PAUL D. · 2001 to 2021
$7.9M
Mechanisms of multi-drug resistant HIV-1 adaptationR21AI054185 · NIAID · AARON DIAMOND AIDS RESEARCH CENTER · PI SIMON, VIVIANA A · 2002 to 2003
$479k
NIAID NIH HHS R01 AI050111NIAID NIH HHS R21 AI054185
6 · The paper itself

Abstract

The HIV-1 Vif protein counteracts the antiviral activity exhibited by the host cytidine deaminases APOBEC3G and APOBEC3F. Here, we show that defective vif alleles can readily be found in HIV-1 isolates and infected patients. Single residue changes in the Vif protein sequence are sufficient to cause the loss of Vif-induced APOBEC3 neutralization. Interestingly, not all the detected defects lead to a complete inactivation of Vif function since some mutants retained selective neutralizing activity against APOBEC3F but not APOBEC3G or vice versa. Concordantly, independently hypermutated proviruses with distinguishable patterns of G-to-A substitution attributable to cytidine deamination induced by APOBEC3G, APOBEC3F, or both enzymes were present in individuals carrying proviruses with completely or partly defective Vif variants. Natural variation in Vif function may result in selective and partial neutralization of cytidine deaminases and thereby promote viral sequence diversification within HIV-1 infected individuals.

Identifiers

PMID16201018
PMCPMC1238741
OpenAlexW2059238079

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.